Key Points
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If there is significant pitting (> 8–10 mm in depth) of the lymphedematous limb, conservative treatment (combined physiotherapy) is indicated to remove the lymph and transfer the lymphedema to a non-pitting state, which indicates that any remaining excess volume consists of lymphedema-induced adipose tissue.
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Liposuction for lymphedema is indicated when pitting is absent or minimal.
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Tumescent solution (1–2L) injected to subcutaneous tissue combined with tourniquet use decreases blood loss.
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A power-assisted liposuction device is useful for shortening the operation time and decreasing the surgeon’s fatigue.
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A custom-made compression sleeve and glove are applied intraoperatively.
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The lifelong use (24 hours/day) of compression garments is mandatory for maintaining the effect of liposuction for limb lymphedema. Changes of the compression garments are required to adjust for limb volume changes.
Introduction
Liposuction techniques have proved to be a valuable tool in various aspects of reconstructive surgery. There is some controversy regarding liposuction as a treatment for late-stage lymphedema. While it is clear that conservative therapies such as complex decongestive therapy (CDT) and controlled compression therapy (CCT) should be tried in the first instance, options for the treatment of late-stage lymphedema that is not responding to this treatment is not so clear. Surgical procedures have been developed and described to address various clinical aspects of the pathophysiology of lymphedema. Microsurgical techniques are promoted to provide physiologic drainage of excessive lymphatic fluid. In many late-stage cases though, adipose tissue deposition and fibrosis are the predominant manifestations of the disease process. Surgical therapies aimed at adipose tissue removal can provide significant symptom relief for affected patients. Liposuction enables complete removal of the deposited adipose tissue leading to complete volume reduction in late stage lymphedema. In addition, liposuction techniques can be useful adjuncts after physiologic procedures to optimize surgical outcomes.
Concepts
Adipose Tissue Hypertrophy
Various possible explanations exist for the hypertrophy of adipose tissue seen in lymphedema. There is a physiological imbalance of blood flow and lymphatic drainage, resulting in the impaired clearance of lipids and their uptake by macrophages. There is increasing support for the view that the fat cell is an endocrine organ and a cytokine-activated cell, and chronic inflammation may play a role in the alterations seen in the disease process. Also, previous research has highlighted the relationship between slow lymph flow and adiposity, as well as that between structural changes in the lymphatic system and adiposity.
Other supported findings for adipose tissue hypertrophy include the following:
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The findings of increased adipose tissue in intestinal segments in patients with inflammatory bowel disease (Crohn’s disease), known as ‘fat wrapping’, have clearly shown that inflammation plays an important role.
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Consecutive analyses of the content of the aspirate removed under bloodless conditions using a tourniquet showed a high content of adipose tissue (mean 90%).
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In Graves’ ophthalmopathy with exophthalmos, adipocyte-related immediate early genes are overexpressed and cysteine-rich, angiogenic inducer 61 may play a role in both orbital inflammation and adipogenesis.
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Tonometry can distinguish if a lymphedematous arm is harder or softer than the normal one. Patients with a harder arm compared with the healthy one have excess adipose tissue.
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Investigation with volume-rendering computer tomography (VR-CT) in 11 patients also showed a significant preoperative increase of adipose tissue of 81% in the swollen arm, followed by a normalization at three months paralleling the complete reduction of the excess volume.
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Analyses with dual-energy X-ray absorptiometry in 18 women with postmastectomy arm lymphedema showed a significant increase of adipose tissue in the nonpitting swollen arm before surgery. Postoperative analyses showed normalization at three months. This effect was seen also at 12 months. These results paralleled the complete reduction of the excess volume.
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A functional inactivation of a single allele of the homeobox gene prospero-related homeobox (Prox)1 led to adult-onset obesity due to abnormal lymph leakage from mispatterned and ruptured lymphatic vessels.
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Parathyroid hormone-like hormone can inhibit adipogenesis and is downregulated both in active and chronic ophthalmopathy, indicating the possibility of an increased risk of adipogenesis.
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Adipogenesis in response to lymphatic fluid stasis is associated with a marked mononuclear cell inflammatory response.
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Lymphatic fluid stasis potently upregulates the expression of fat differentiation markers both spatially and temporally.
Clinicians often believe that the swelling of a lymphedematous extremity is purely due to the accumulation of lymph fluid, which can be removed by the use of noninvasive conservative regimens, such as CDT and CCT. These therapies work well when the excess swelling consists of accumulated lymph, but do not work when the excess volume is dominated by adipose tissue and related fibrosis. Microsurgical procedures using lymphovenous shunts, lymph vessel transplantation, and vascularized lymph node transfer do not remove adipose tissue.
Regional Anatomy
The superficial lymphatic system consists of a fine dermal network draining to the lymphatics surrounding the major superficial veins, such as the cephalic vein or great saphenous vein. The deep lymphatic system is located under the muscle fascia and follows the major blood vessels. The superficial and deep lymphatic system drain to regional lymph node basins located along the lymphatic vessels (popliteal, inguinal fossae, and axilla), transporting the lymph through the lymph nodes on its way to the larger lymphatic vessels and ducts (the thoracic duct on the left side and the right lymphatic duct on the right side), which ultimately transports the lymph to the venous system by emptying into the venous angles in the neck (junction of the internal jugular vein and the subclavian vein).
Starling’s equation describes how the transcapillary exchange is regulated. Changes in the hydrostatic and colloid osmotic pressures affect the fluid exchange between blood and tissue, and thus the amount of interstitial fluid. Knowledge of this regulation is the basis of treating patients with edema. See Box 12.1 .
Jv = Kf ( ( Pc − Pt ) − K d ( Poc − Pot ) )
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